99 research outputs found

    Event related potentials reveal that increasing perceptual load leads to increased responses for target stimuli and decreased responses for irrelevant stimuli

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    This Document is Protected by copyright and was first published by Frontiers. All rights reserved. It is reproduced with permission.Peer reviewedPublisher PD

    Enhanced Tactile Performance at the Destination of an Upcoming Saccade

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    AbstractPrevious work has demonstrated that upcoming saccades influence visual [1, 2] and auditory [3] performance even for stimuli presented before the saccade is executed. These studies suggest a close relationship between saccade generation and visual/auditory attention. Furthermore, they provide support for Rizzolatti et al.'s [4, 5] premotor model of attention, which suggests that the same circuits involved in motor programming are also responsible for shifts in covert orienting (shifting attention without moving the eyes or changing posture). In a series of experiments, we demonstrate that saccade programming also affects tactile perception. Participants made speeded saccades to the left and right side as well as tactile discriminations of up versus down. The first experiment demonstrates that participants were reliably faster at responding to tactile stimuli near the location of upcoming saccades. In our second experiment, we had the subjects cross their hands and demonstrated that the effect occurs in visual space (rather than the early representations of touch). In our third experiment, the tactile events usually occurred on the opposite side of upcoming eye movement. We found that the benefit at the saccade target location vanished, suggesting that this shift is not obligatory but that it may be vetoed on the basis of expectation

    Towards incorporation of blue carbon in Falkland Islands marine spatial planning: a multi-tiered approach

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    Ecosystem-based conservation that includes carbon sinks, alongside a linked carbon credit system, as part of a nature-based solution to combating climate change, could help reduce greenhouse gas levels and therefore the impact of their emissions. Blue carbon habitats and pathways can also facilitate biodiversity retention, aiding sustainable fisheries and island economies. However, robust blue carbon research is often limited at the scale of regional governance and management, lacking both incentives and facilitation of policy-integration. The remote and highly biodiverse coastal ecosystems and surrounding continental shelf can be used to better inform long-term ecosystem-based management in the vast South Atlantic Ocean and sub-Antarctic, to synergistically protect both unique biodiversity and inform on the magnitude of nature-based benefits they provide. Understanding key ecosystem information such as their location, extent, and condition of habitat types, will be critical in understanding carbon pathways to sequestration, threats to this, and vulnerability. This paper considers the current status of blue carbon data and information available, and what is still required before blue carbon can be used as a conservation management tool integrated in national Marine Spatial Planning (MSP) initiatives. Our research indicates that the data and information gathered has enabled baselines for a number of different blue carbon ecosystems, and indicated potential threats and vulnerability that need to be managed. However, significant knowledge gaps remain across habitats, such as salt marsh, mudflats and the mesophotic zones, which hinders meaningful progress on the ground where it is needed most

    Aldosterone Antagonists in Monotherapy Are Protective against Streptozotocin-Induced Diabetic Nephropathy in Rats

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    Angiotensin converting enzyme inhibitors (ACEi) and angiotensin II receptor blockers (ARB) are the standard clinical therapy of diabetic nephropathy (DN), while aldosterone antagonists are only used as adjuncts. Previously in experimental DN we showed that Na/K ATPase (NKA) is mislocated and angiotensin II leads to superimposed renal progression. Here we investigated the monotherapeutic effect of aldosterone blockers on the progression of DN and renal NKA alteration in comparison to ACEi and ARBs. Streptozotocin-diabetic rats developing DN were treated with aldosterone antagonists; ACEi and ARB. Renal function, morphology, protein level and tubular localization of NKA were analyzed. To evaluate the effect of high glucose per se; HK-2 proximal tubular cells were cultured in normal or high concentration of glucose and treated with the same agents. Aldosterone antagonists were the most effective in ameliorating functional and structural kidney damage and they normalized diabetes induced bradycardia and weight loss. Aldosterone blockers also prevented hyperglycemia and diabetes induced increase in NKA protein level and enzyme mislocation. A monotherapy with aldosterone antagonists might be as, or more effective than ACEi or ARBs in the prevention of STZ-induced DN. Furthermore the alteration of the NKA could represent a novel pathophysiological feature of DN and might serve as an additional target of aldosterone blockers

    Dysregulation of CXC motif ligand 10 during aging and association with cognitive performance

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    Chronic low-grade inflammation during aging (inflammaging) is associated with cognitive decline and neurodegeneration, however, the mechanisms underlying inflammaging are unclear. We studied a population (n = 361) of healthy young and old adults from the MyoAge cohort. Peripheral levels of C-X-C motif chemokine 10 (CXCL10) was found to be higher in older adults, compared with young, and negatively associated with working memory performance. This coincided with an age-related reduction in blood DNA methylation at specific CpGs within the CXCL10 gene promoter. In vitro analysis supported the role of DNA methylation in regulating CXCL10 transcription. A polymorphism (rs56061981) that altered methylation at one of these CpG sites further associated with working memory performance in two independent aging cohorts. Studying prefrontal cortex samples, we found higher CXCL10 protein levels in those with Alzheimer’s disease, compared to aged controls. These findings support the association of peripheral inflammation, as demonstrated by CXCL10, in aging and cognitive decline. We reveal age-related epigenetic and genetic factors which contribute to the dysregulation of CXCL10

    Nitric oxide deficiency in chronic kidney disease

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    Importance of nitric oxide in the control of renal hemodynamics

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    Importance of nitric oxide in the control of renal hemodynamics. The kidney vasculature is under tonic control by nitric oxide (NO) and in cortex, NO controls RA and Kf. Systemic NO inhibition leads to systemic hypertension, increases in RE, mediated by Ang II and ET, and direct effects on RA and Kf. The relationship between NO and other vasoconstrictor systems is variable. In the conscious relaxed animal, vasoconstrictor activity is low, yet acute NO inhibition leads to pressor and renal vasoconstrictor reponses. At physiologic levels, ET unexpectedly is a renal vasodilator, possibly via NO generation at RA. When vasoconstrictor activity is high, NO is very important in maintenance of renal perfusion. Chronic L-NAME produces dose dependent systemic and glomerular capillary hypertension and eventual proteinuria and glomerular damage. NO deficiency is key in this process, although the hypertension becomes refractory to L-arginine administration and dependent on Ang II and the SNS, by mechanisms not yet defined. In contrast, the renal vasculature remains fully responsive to L-arginine, suggesting that pressor and renal vascular responses to chronic NO inhibition are separately regulated. NO generated from iNOS does not normally control BP or renal hemodynamics. The relative contributions of NO from bNOS and eNOS, and importance of NOS in different locations in the kidney, remain to be determined

    Total nitric oxide production is low in patients with chronic renal disease

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    Total nitric oxide production is low in patients with chronic renal disease.BackgroundA deficiency of the endogenous vasodilator nitric oxide (NO) has been implicated as a potential cause of hypertension in chronic renal disease (CRD) patients. This study was conducted to determine whether 24-hour NOX (NO2 and NO3) excretion (a qualitative index of total NO production) is reduced in patients with CRD.MethodsMeasurements were made in 13 CRD patients and 9 normotensive healthy controls after 48 hours on a controlled low-NOX diet. Urine was collected over the second 24-hour period for analysis of 24-hour NOX, and cGMP and blood drawn at the completion. Plasma levels of arginine (the substrate for endogenous renal NO synthesis), citrulline (substrate for renal arginine synthesis), and the endogenous NO synthesis inhibitor asymmetrical dimethylarginine (ADMA) and its inert isomer and symmetrical dimethylarginine (SDMA) were also determined.ResultsSystolic blood pressure was higher in CRD patients (12 of whom were already on antihypertensive therapy) than in controls (P < 0.05). Twenty-four–hour urinary NOX excretion was low in CRD patients compared with controls despite similar dietary NO intake, suggesting that net endogenous NO production is decreased in renal disease. In contrast, the 24-hour urinary cGMP did not correlate with UNOXV. Plasma citrulline was increased in CRD patients, possibly reflecting reduced conversion of citrulline to arginine. Plasma arginine was not different, and plasma ADMA levels were elevated in CRD versus controls, changes that would tend to lower NO synthase.ConclusionThese results suggest that NO production is low in CRD patients and may contribute to hypertension and disease progression in CRD
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